Upper Gastrointestinal Bleeding
- Author: Maurice A Cerulli, MD, FACP, FACG, FASGE, AGAF; Chief Editor: BS Anand, MD more...
Acute gastrointestinal bleeding is a potentially life-threatening abdominal emergency that remains a common cause of hospitalization. Upper gastrointestinal bleeding (UGIB) is defined as bleeding derived from a source proximal to the ligament of Treitz.
The image below depicts an ulcer with active bleeding.
Signs and symptoms
Signs and symptoms of acute upper GI bleeding include the following:
Diffuse abdominal pain
See Clinical Presentation for more detail.
Workup includes the following:
Orthostatic blood pressure
Complete blood count with differential
Type and crossmatch blood
Basic metabolic profile, blood urea nitrogen, and coagulation profile
Angiography (if bleeding persists and endoscopy fails to identify a bleeding site)
Computed tomography scanning and ultrasonography may be indicated for the evaluation of the following :
Liver disease with cirrhosis
Cholecystitis with hemorrhage
Pancreatitis with pseudocyst and hemorrhage
See Workup for more detail.
Treatment includes the following:
Secure the airway
Insert bilateral, 16-gauge (minimum), upper extremity, peripheral intravenous lines
Replace each milliliter of blood loss with 3 mL of crystalloid fluid
In patients with severe coexisting medical illnesses, pulmonary artery catheter insertion for monitoring hemodynamic cardiac performance
Foley catheter placement for continuous evaluation of urinary output as a guide to renal perfusion
Endoscopic hemostatic therapy for bleeding ulcers and varices
Surgical repair of perforated viscus
For high-risk peptic ulcer patients, high-dose intravenous proton pump inhibitors
Indications for surgery in patients with bleeding peptic ulcers include the following:
Severe, life-threatening hemorrhage not responsive to resuscitative efforts
Failure of medical therapy and endoscopic hemostasis with persistent recurrent bleeding
A coexisting reason for surgery (eg, perforation, obstruction, malignancy)
Prolonged bleeding, with loss of 50% or more of the patient's blood volume
A second hospitalization for peptic ulcer hemorrhage
Acute gastrointestinal (GI) bleeding is a potentially life-threatening abdominal emergency that remains a common cause of hospitalization.[3, 4] Upper gastrointestinal bleeding (UGIB) is defined as bleeding derived from a source proximal to the ligament of Treitz.
The incidence of UGIB is approximately 100 cases per 100,000 population per year. Bleeding from the upper GI tract is approximately 4 times more common than bleeding from the lower GI tract and is a major cause of morbidity and mortality. Mortality rates from UGIB are 6-10% overall. (See Epidemiology, below.)
The diagnosis of and therapy for nonvariceal upper gastrointestinal bleeding (UGIB) has evolved since the late 20th century from passive diagnostic esophagogastroduodenoscopy with medical therapy until surgical intervention was needed to active intervention with endoscopic techniques followed by angiographic and surgical approaches if endoscopic therapy fails. (See Workup and Treatment and Management, below.)
Variceal hemorrhage is not discussed in this article because the underlying mechanisms of bleeding are different and require different therapies.
The underlying mechanisms of nonvariceal bleeding involve either arterial hemorrhage, such as in ulcer disease and mucosal deep tears, or low-pressure venous hemorrhage, as in telangiectasias and angioectasias. In variceal hemorrhage, the underlying pathophysiology is due to elevated portal pressure transmitted to esophageal and gastric varices and resulting in portal gastropathy. A bleeding ulcer is seen below. (See Etiology, below.)
Go to Pediatric Gastrointestinal Bleeding for complete information on this topic.
In patients with UGIB, comorbid illness, rather than actual bleeding, is the major cause of death. Comorbid illness has been noted in 50.9% of patients, with similar occurrences in males (48.7%) and females (55.4%).
One or more comorbid illnesses have been noted in 98.3% of mortalities in UGIB; in 72.3% of patients, comorbid illnesses have been noted as the primary cause of death.[8, 9] (See Epidemiology and Prognosis, below.)
Significant comorbidities have become more prevalent as the patient population with UGIB has become progressively older. In a retrospective chart review by Yavorski et al, 73.2% of deaths occurred in patients older than 60 years. (See Epidemiology and Prognosis, below.)
Rebleeding or continued bleeding is associated with increased mortality; therefore, differentiating the patient with a low probability of rebleeding and little comorbidity from the patient at high risk for rebleeding with serious comorbidities is imperative. (See Clinical Presentation and Workup, below.)
Peptic ulcer disease and UGIB
Peptic ulcer disease (PUD) remains the most common cause of UGIB. In a literature review involving more than 10,000 patients with UGIB, PUD was responsible for 27-40% of all bleeding episodes. High-risk patient populations at risk for PUD include those with a history of alcohol abuse, chronic renal failure, and/or nonsteroidal anti-inflammatory drug (NSAID) use.
Peptic ulcer disease is strongly associated with Helicobacter pylori infection. The organism causes disruption of the mucous barrier and has a direct inflammatory effect on gastric and duodenal mucosa, reducing mucosal defenses and increasing back diffusion of acid by loosening the tight cellular junctions. (Rates of H pylori infection are reportedly lower in patients with complicated ulcer disease than in patients with uncomplicated ulcers. Hosking et al reported a 71% incidence of H pylori infection in patients with bleeding duodenal ulcers; patients with nonbleeding ulcers had an incidence of 93%.) This discrepancy may be due to the decrease in sensitivity of biopsy in patients with ulcer bleeding.
Eradication of H pylori been demonstrated to reduce the risk of recurrent ulcers and, thus, recurrent ulcer hemorrhage after the initial episode. In fact, the proportion of UGIB cases caused by peptic ulcer disease has declined, a phenomenon that is believed to be due to the use of proton pump inhibitors (PPIs) and H pylori therapy.
Duodenal ulcers are more common than gastric ulcers, but the incidence of bleeding is identical for both. In most cases, the bleeding is caused by the erosion of an artery at the base of the ulcer. In approximately 80% of patients, bleeding from a peptic ulcer stops spontaneously.
Initial endoscopic attempts to maintain hemostasis have a high failure rate. Bleeding vessels larger than 1.5 mm in diameter are associated with an increased mortality rate due to the difficulty in producing adequate hemostasis with thermal probes.
A minority of patients experience recurrent bleeding after endoscopic therapy, and these cases are usually associated with risk factors for rebleeding. These factors include age older than 60 years, the presence of shock upon admission, coagulopathy, active pulsatile bleeding, and the presence of cardiovascular disease. (The appearance of the ulcer at the time of endoscopy provides important information regarding the risk of rebleeding.) These circumstances are associated with a poorer prognosis and a higher mortality rate.
Despite the dangers associated with a bleeding peptic ulcer, a study by Sung et al of 10,428 cases of such bleeding (in 9,375 patients) found that most deaths were not caused by it. Of the 577 deaths that occurred in the cohort, almost 80% resulted from other causes, including multiorgan failure, pulmonary conditions, and terminal malignancy. The authors concluded that the management of patients with peptic ulcers should focus not only on hemostasis but also on lowering the risk of multiorgan failure and cardiopulmonary death.
Recurrent bleeding risk in peptic ulcers
Forrest et al were the first to classify the stigmata of hemorrhage from peptic ulcers. Based on these classifications, the risk of recurrent bleeding can be predicted. The ulcers at highest risk for rebleeding are those that involve active arterial bleeding or those with a visible, protuberant, nonbleeding vessel at the base of the ulcer. The study not only correlated the incidence of rebleeding with the stigmata of recent bleeding and the endoscopic appearance of an ulcer, but also determined prognostic information regarding the need for surgery. Mortality was also correlated with these factors.
In patients with H pylori infection, the rate of recurrent bleeding is extremely low. This is why documenting the presence of H pylori and aggressively treating the infection are important.
Patients who are not infected with H pylori may require a subsequent acid-lowering surgical procedure or long-term medical therapy for recurrent ulcer disease and bleeding.
Other causes of UGIB
Other major causes of UGIB are mucosal tears of the esophagus or fundus (Mallory-Weiss tear), erosive gastritis, erosive esophagitis, Dieulafoy lesion, gastric cancer, and ulcerated gastric leiomyoma.
Patients with chronic liver disease and portal hypertension are at an increased risk for variceal hemorrhage and portal gastropathy in addition to ulcer hemorrhage.
Rare causes of UGIB include aortoenteric fistula, gastric antral vascular ectasia, angiectasias, and Osler-Weber-Rendu syndrome.
An aortoenteric fistula results from the erosion of the aortic graft into the bowel lumen, usually at the third or fourth portion of the duodenum. The result is a direct communication between the aortic graft lumen and the bowel lumen. Most aortoenteric fistulas involve the proximal aortic anastomotic suture line.
UGIB can also result from acute stress gastritis, a disease process characterized by diffuse superficial mucosal erosions that appear as discrete areas of erythema. The bleeding is usually mild and self-limiting and rarely progresses to life-threatening hemorrhage.
In intensive care unit (ICU) patients, the incidence of clinically significant GI bleeding (eg, hypotension, transfusion) from acute stress gastritis was found to be 1.5%. Stress gastritis and mucosal ulceration are historically associated with (1) head injuries with associated elevations in intracranial pressure and (2) burn injuries. These stress ulcers are called Cushing ulcers and Curling ulcers, respectively.
Angiodysplasia of the upper GI tract accounts for 2-4% of bleeding lesions. The condition is also a cause of lower GI bleeding in 6% of cases. The lesion is a vascular malformation that represents an abnormal dilation of mucosal and submucosal vessels.
Histologically, angiodysplasias are dilated, thin-walled vascular channels that appear macroscopically as a cluster of cherry spots. When located in the upper GI tract, they most commonly involve the stomach and duodenum. The lesions can be acquired or congenital, as in hereditary hemorrhagic telangiectasia and Rendu-Osler-Weber syndrome.
The acquired angiodysplasias are commonly found in patients with chronic renal failure requiring hemodialysis and with aortic valvular disease (especially aortic stenosis). Other diseases, such as cirrhosis and von Willebrand disease, are associated with a higher frequency of angiodysplasias. Most lesions are smaller than 1 cm in diameter and can be multiple in 66% of patients.
Bleeding peptic ulcers account for the majority of patients presenting with acute upper gastrointestinal bleeding (UGIB). As previously mentioned, peptic ulcer disease is strongly associated with H pylori infection. The organism causes disruption of the mucous barrier and has a direct inflammatory effect on gastric and duodenal mucosa.
In cases of ulcer-associated UGIB, as the ulcer burrows deeper into the gastroduodenal mucosa, the process causes weakening and necrosis of the arterial wall, leading to the development of a pseudoaneurysm. The weakened wall ruptures, producing hemorrhage.
The flow through a vessel varies with the fourth power of the radius; thus, small increases in vessel size can mean much larger amounts of blood flow and bleeding, with more severe hypotension and more complications, especially in older patients.
Visible vessels usually range from 0.3-1.8 mm.
Exsanguinating hemorrhage has been reported from larger vessels. The larger vessels are located deeper in the gastric and duodenal submucosa and serosa. Larger branches of the left gastric artery are found high on the lesser curvature, while the pancreatoduodenal artery and its major branches are located posteroinferiorly in the duodenal bulb.
During vomiting, the lower esophagus and upper stomach are forcibly inverted. Vomiting attributable to any cause can lead to a mucosal tear of the lower esophagus or upper stomach. The depth of the tear determines the severity of the bleeding. Rarely, vomiting can result in esophageal rupture (Boerhaave syndrome), leading to bleeding, mediastinal air entry, left pleural effusion (salivary amylase can be present) or left pulmonary infiltrate, and subcutaneous emphysema.
Mallory-Weiss tears in UGIB
Mallory-Weiss tears account for 15% of acute upper GI hemorrhage. Kenneth Mallory and Soma Weiss first described the syndrome in 1929. The massive UGIB results from a tear in the mucosa of the gastric cardia.
This linear mucosal laceration is the result of forceful vomiting, retching, coughing, or straining. These actions create a rapid increase in the gradient between intragastric and intrathoracic pressures, leading to a gastric mucosal tear from the forceful distention of the gastroesophageal junction. In 80-90% of cases, this is a single, 1.75- to 2.5-cm mucosal tear along the lesser curve of the stomach just distal to the gastroesophageal junction.
Go to Mallory-Weiss Tear for complete information on this topic.
Acute stress gastritis in UGIB
Acute stress gastritis results from predisposing clinical conditions that have the potential to alter the local mucosal protective barriers, such as mucus, bicarbonate, blood flow, and prostaglandin synthesis. Any disease process that disrupts the balance of these factors results in diffuse gastric mucosal erosions.
This is most commonly observed in patients who have undergone episodes of shock, multiple trauma, acute respiratory distress syndrome, systemic respiratory distress syndrome, acute renal failure, and sepsis.
The principal mechanisms involved are decreased splanchnic mucosal blood flow and altered gastric luminal acidity.
Dieulafoy lesions in UGIB
The Dieulafoy lesion, first described in 1896, is a vascular malformation of the proximal stomach, usually within 6 cm of the gastroesophageal junction along the lesser curvature of the stomach. However, it can occur anywhere along the GI tract. This lesion accounts for 2-5% of acute UGIB episodes.
Endoscopically, the lesion appears as a large submucosal vessel that has become ulcerated. Because of the large size of the vessel, bleeding can be massive and brisk. The vessel rupture usually occurs in the setting of chronic gastritis, which may induce necrosis of the vessel wall. Alcohol consumption is reportedly associated with the Dieulafoy lesion.
In a review of 149 cases, the Dieulafoy lesion mostly occurred in men and mostly in those in their third to tenth decade.
NSAIDs in UGIB
NSAIDs cause gastric and duodenal ulcers by inhibiting cyclooxygenase, which causes decreased mucosal prostaglandin synthesis and results in impaired mucosal defenses. Daily NSAID use causes an estimated 40-fold increase in gastric ulcer creation and an 8-fold increase in duodenal ulcer creation.
Long-term NSAID use is associated with a 20% incidence in the development of mucosal ulceration. Medical therapy includes avoiding the ulcerogenic drug and beginning a histamine-2 (H2)–receptor antagonist or a proton pump inhibitor that provides mucosal protection.
Annually, approximately 100,000 patients are admitted to US hospitals for therapy for UGIB. In the United Kingdom, UGIB accounts for 70,000 hospital admissions each year, with the majority of cases nonvariceal in origin.
UGIB is a common occurrence throughout the world. In France, a report concludes that the mortality from UGIB has decreased from about 11% to 7%; however, a similar report from Greece finds no decrease in mortality. In a nationwide study from Spain, UGIB was 6 times more common than lower GI bleeding.
The incidence of UGIB is 2-fold greater in males than in females, in all age groups; however, the death rate is similar in both sexes.
The population with UGIB has become progressively older, with a concurrent increase in significant comorbidities that increase mortality. Mortality increases with older age (>60 y), in both males and females.
As previously mentioned, age older than 60 years is an independent marker for a poor outcome in upper gastrointestinal bleeding (UGIB), with the mortality rate ranging from 12-25% in this group of patients.
The American Society for Gastrointestinal Endoscopy (ASGE) grouped patients with UGIB according to age and correlated age category to the risk of mortality. The ASGE found a mortality rate of 3.3% for patients aged 21-31 years, a rate of 10.1% for those aged 41-50 years, and a rate of 14.4% for those aged 71-80 years.
The following risk factors are associated with an increased mortality, recurrent bleeding, the need for endoscopic hemostasis, or surgery[14, 26] :
Age older than 60 years
Active bleeding (eg, witnessed hematemesis, red blood per nasogastric tube, fresh blood per rectum)
Red blood cell transfusion greater than or equal to 6 units
Inpatient at time of bleed
Patients who present in hemorrhagic shock have a mortality rate of up to 30%.
al-Assi MT, Genta RM, Karttunen TJ, Graham DY. Ulcer site and complications: relation to Helicobacter pylori infection and NSAID use. Endoscopy. 1996 Feb. 28(2):229-33. [Medline].
Frattaroli FM, Casciani E, Spoletini D, Polettini E, Nunziale A, Bertini L, et al. Prospective study comparing multi-detector row CT and endoscopy in acute gastrointestinal bleeding. World J Surg. 2009 Oct. 33(10):2209-17. [Medline].
Lam KL, Wong JC, Lau JY. Pharmacological treatment in upper gastrointestinal bleeding. Curr Treat Options Gastroenterol. 2015 Dec. 13 (4):369-76. [Medline].
Curdia Goncalves T, Rosa B, Cotter J. New insights on an old medical emergency: non-portal hypertension related upper gastrointestinal bleeding. Rev Esp Enferm Dig. 2016 Mar 4. 108:[Medline].
Lirio RA. Management of upper gastrointestinal bleeding in children: variceal and nonvariceal. Gastrointest Endosc Clin N Am. 2016 Jan. 26 (1):63-73. [Medline].
Fallah MA, Prakash C, Edmundowicz S. Acute gastrointestinal bleeding. Med Clin North Am. 2000 Sep. 84(5):1183-208. [Medline].
Pongprasobchai S, Nimitvilai S, Chasawat J, Manatsathit S. Upper gastrointestinal bleeding etiology score for predicting variceal and non-variceal bleeding. World J Gastroenterol. 2009 Mar 7. 15(9):1099-104. [Medline]. [Full Text].
Straube S, Tramèr MR, Moore RA, Derry S, McQuay HJ. Mortality with upper gastrointestinal bleeding and perforation: effects of time and NSAID use. BMC Gastroenterol. 2009 Jun 5. 9:41. [Medline]. [Full Text].
Yavorski RT, Wong RK, Maydonovitch C, Battin LS, Furnia A, Amundson DE. Analysis of 3,294 cases of upper gastrointestinal bleeding in military medical facilities. Am J Gastroenterol. 1995 Apr. 90(4):568-73. [Medline].
Stabile BE, Stamos MJ. Surgical management of gastrointestinal bleeding. Gastroenterol Clin North Am. 2000 Mar. 29(1):189-222. [Medline].
Cheung FK, Lau JY. Management of massive peptic ulcer bleeding. Gastroenterol Clin North Am. 2009 Jun. 38(2):231-43. [Medline].
Tiriveedhi K, Simon J, Cerulli MA. Does Gastric Lavage Reduce the Detection of Helicobacter Pylori in the Biopsy Specimens?. Gastrointest Endosc. 2007. 67:Abstract 239.
Boonpongmanee S, Fleischer DE, Pezzullo JC, Collier K, Mayoral W, Al-Kawas F, et al. The frequency of peptic ulcer as a cause of upper-GI bleeding is exaggerated. Gastrointest Endosc. 2004 Jun. 59(7):788-94. [Medline].
Elmunzer BJ, Young SD, Inadomi JM, Schoenfeld P, Laine L. Systematic review of the predictors of recurrent hemorrhage after endoscopic hemostatic therapy for bleeding peptic ulcers. Am J Gastroenterol. 2008 Oct. 103(10):2625-32; quiz 2633. [Medline].
Sung JJ, Tsoi KK, Ma TK, Yung MY, Lau JY, Chiu PW. Causes of mortality in patients with peptic ulcer bleeding: a prospective cohort study of 10,428 cases. Am J Gastroenterol. 2010 Jan. 105(1):84-9. [Medline].
Corson JD, Williamson RCN, eds. Surgery. London, UK: Mosby-Year Book; 2001.
Stollman N, Metz DC. Pathophysiology and prophylaxis of stress ulcer in intensive care unit patients. J Crit Care. 2005 Mar. 20(1):35-45. [Medline].
Cameron JL, ed. Current Surgical Therapy. 5th ed. St. Louis, Mo: Mosby-Year Book; 1995.
Jensen DM, Machicado GA, Hirabayashi K. Randomized controlled study of 3 different types of hemoclips for hemostasis of bleeding canine acute gastric ulcers. Gastrointest Endosc. 2006 Nov. 64(5):768-73. [Medline].
Larson G, Schmidt T, Gott J, Bond S, O'Connor CA, Richardson JD. Upper gastrointestinal bleeding: predictors of outcome. Surgery. 1986 Oct. 100(4):765-73. [Medline].
Reilly HF 3rd, al-Kawas FH. Dieulafoy's lesion. Diagnosis and management. Dig Dis Sci. 1991 Dec. 36(12):1702-7. [Medline].
Pilotto A, Maggi S, Noale M, Franceschi M, Parisi G, Crepaldi G. Development and validation of a new questionnaire for the evaluation of upper gastrointestinal symptoms in the elderly population: a multicenter study. J Gerontol A Biol Sci Med Sci. 2010 Feb. 65(2):174-8. [Medline].
Jairath V, Desborough MJ. Modern-day management of upper gastrointestinal haemorrhage. Transfus Med. 2015 Dec 28. [Medline].
Lanas A, Perez-Aisa MA, Feu F, Ponce J, Saperas E, Santolaria S, et al. A nationwide study of mortality associated with hospital admission due to severe gastrointestinal events and those associated with nonsteroidal antiinflammatory drug use. Am J Gastroenterol. 2005 Aug. 100(8):1685-93. [Medline].
Peter DJ, Dougherty JM. Evaluation of the patient with gastrointestinal bleeding: an evidence based approach. Emerg Med Clin North Am. 1999 Feb. 17(1):239-61, x. [Medline].
Adler DG, Leighton JA, Davila RE, Hirota WK, Jacobson BC, Qureshi WA, et al. ASGE guideline: The role of endoscopy in acute non-variceal upper-GI hemorrhage. Gastrointest Endosc. 2004 Oct. 60(4):497-504. [Medline].
Laine L, Shah A. Randomized trial of urgent vs. elective colonoscopy in patients hospitalized with lower GI bleeding. Am J Gastroenterol. 2010 Dec. 105(12):2636-41; quiz 2642. [Medline].
American College of Surgeons Committee on Trauma. Advanced Trauma Life Support Course Manual. Chicago, Ill: American College of Surgeons; 1997.
Bornman PC, Theodorou NA, Shuttleworth RD, Essel HP, Marks IN. Importance of hypovolaemic shock and endoscopic signs in predicting recurrent haemorrhage from peptic ulceration: a prospective evaluation. Br Med J (Clin Res Ed). 1985 Jul 27. 291(6490):245-7. [Medline]. [Full Text].
Silverstein FE, Gilbert DA, Tedesco FJ, Buenger NK, Persing J. The national ASGE survey on upper gastrointestinal bleeding. II. Clinical prognostic factors. Gastrointest Endosc. 1981 May. 27(2):80-93. [Medline].
Villanueva C, Colomo A, Bosch A, Concepción M, Hernandez-Gea V, Aracil C, et al. Transfusion strategies for acute upper gastrointestinal bleeding. N Engl J Med. 2013 Jan 3. 368(1):11-21. [Medline].
Waknine Y. GI Bleeds: Withholding Transfusions Boosts Survival. Medscape Medical News. January 15, 2013. [Full Text].
Transfusion Strategies for Acute Upper Gastrointestinal Bleeding. N Engl J Med. 2013 May 16. [Medline].
[Guideline] Scottish Intercollegiate Guidelines Network (SIGN). Management of acute upper and lower gastrointestinal bleeding. A national clinical guideline. Edinburgh (Scotland): Scottish Intercollegiate Guidelines Network (SIGN); 2008 Sep. (SIGN publication; no. 105): [Full Text].
Peloquin JM, Seraj SM, King LY, Campbell EJ, Ananthakrishnan AN, Richter JM. Diagnostic and therapeutic yield of endoscopy in patients with elevated INR and gastrointestinal bleeding. Am J Med. 2015 Dec 20. [Medline].
[Guideline] Schenker MP, Majdalany BS, Funaki BS, et al; and Expert Panel on Vascular Imaging and Interventional Radiology. ACR Appropriateness Criteria® upper gastrointestinal bleeding. [online publication]. Reston (VA): American College of Radiology (ACR); 2010. [Full Text].
Chandran S, Testro A, Urquhart P, La Nauze R, Ong S, Shelton E, et al. Risk stratification of upper GI bleeding with an esophageal capsule. Gastrointest Endosc. 2013 Feb 26. [Medline].
Iwasaki H, Shimura T, Yamada T, Aoki M, Nomura S, Kusakabe A, et al. Novel Nasogastric Tube-Related Criteria for Urgent Endoscopy in Nonvariceal Upper Gastrointestinal Bleeding. Dig Dis Sci. 2013 May 22. [Medline].
Monteiro S, Goncalves TC, Magalhaes J, Cotter J. Upper gastrointestinal bleeding risk scores: Who, when and why?. World J Gastrointest Pathophysiol. 2016 Feb 15. 7 (1):86-96. [Medline].
Baradarian R, Ramdhaney S, Chapalamadugu R, Skoczylas L, Wang K, Rivilis S, et al. Early intensive resuscitation of patients with upper gastrointestinal bleeding decreases mortality. Am J Gastroenterol. 2004 Apr. 99(4):619-22. [Medline].
Kaplan LJ, McPartland K, Santora TA, Trooskin SZ. Start with a subjective assessment of skin temperature to identify hypoperfusion in intensive care unit patients. J Trauma. 2001 Apr. 50(4):620-7; discussion 627-8. [Medline].
Green FW Jr, Kaplan MM, Curtis LE, Levine PH. Effect of acid and pepsin on blood coagulation and platelet aggregation. A possible contributor prolonged gastroduodenal mucosal hemorrhage. Gastroenterology. 1978 Jan. 74(1):38-43. [Medline].
Lau JY, Leung WK, Wu JC, et al. Omeprazole before endoscopy in patients with gastrointestinal bleeding. N Engl J Med. 2007 Apr 19. 356(16):1631-40. [Medline].
Barkun AN, Herba K, Adam V, Kennedy W, Fallone CA, Bardou M. High-dose intravenous proton pump inhibition following endoscopic therapy in the acute management of patients with bleeding peptic ulcers in the USA and Canada: a cost-effectiveness analysis. Aliment Pharmacol Ther. 2004 Mar 1. 19(5):591-600. [Medline].
Laine L, Shah A, Bemanian S. Intragastric pH with oral vs intravenous bolus plus infusion proton-pump inhibitor therapy in patients with bleeding ulcers. Gastroenterology. 2008 Jun. 134(7):1836-41. [Medline].
Leontiadis GI, Sharma VK, Howden CW. Proton pump inhibitor therapy for peptic ulcer bleeding: Cochrane collaboration meta-analysis of randomized controlled trials. Mayo Clin Proc. 2007 Mar. 82(3):286-96. [Medline].
Lau JY, Sung JJ, Lam YH, et al. Endoscopic retreatment compared with surgery in patients with recurrent bleeding after initial endoscopic control of bleeding ulcers. N Engl J Med. 1999 Mar 11. 340(10):751-6. [Medline].
Cooper GS, Chak A, Way LE, Hammar PJ, Harper DL, Rosenthal GE. Early endoscopy in upper gastrointestinal hemorrhage: associations with recurrent bleeding, surgery, and length of hospital stay. Gastrointest Endosc. 1999 Feb. 49(2):145-52. [Medline].
[Guideline] Barkun AN, Bardou M, Kuipers EJ, et al. International consensus recommendations on the management of patients with nonvariceal upper gastrointestinal bleeding. Ann Intern Med. 2010 Jan 19. 152(2):101-13. [Medline]. [Full Text].
Matsui S, Kamisako T, Kudo M, Inoue R. Endoscopic band ligation for control of nonvariceal upper GI hemorrhage: comparison with bipolar electrocoagulation. Gastrointest Endosc. 2002 Feb. 55(2):214-8. [Medline].
Giday SA, Kim Y, Krishnamurty DM, et al. Long-term randomized controlled trial of a novel nanopowder hemostatic agent (TC-325) for control of severe arterial upper gastrointestinal bleeding in a porcine model. Endoscopy. 2011 Apr. 43(4):296-9. [Medline].
Vargas HE, Gerber D, Abu-Elmagd K. Management of portal hypertension-related bleeding. Surg Clin North Am. 1999 Feb. 79(1):1-22. [Medline].
Cipolletta L, Bianco MA, Marmo R, Rotondano G, Piscopo R, Vingiani AM, et al. Endoclips versus heater probe in preventing early recurrent bleeding from peptic ulcer: a prospective and randomized trial. Gastrointest Endosc. 2001 Feb. 53(2):147-51. [Medline].
Lin HJ, Hsieh YH, Tseng GY, Perng CL, Chang FY, Lee SD. A prospective, randomized trial of endoscopic hemoclip versus heater probe thermocoagulation for peptic ulcer bleeding. Am J Gastroenterol. 2002 Sep. 97(9):2250-4. [Medline].
Saltzman JR, Strate LL, Di Sena V, Huang C, Merrifield B, Ookubo R, et al. Prospective trial of endoscopic clips versus combination therapy in upper GI bleeding (PROTECCT--UGI bleeding). Am J Gastroenterol. 2005 Jul. 100(7):1503-8. [Medline].
Bini EJ, Cohen J. Endoscopic treatment compared with medical therapy for the prevention of recurrent ulcer hemorrhage in patients with adherent clots. Gastrointest Endosc. 2003 Nov. 58(5):707-14. [Medline].
Freeman ML, Cass OW, Peine CJ, Onstad GR. The non-bleeding visible vessel versus the sentinel clot: natural history and risk of rebleeding. Gastrointest Endosc. 1993 May-Jun. 39(3):359-66. [Medline].
Poxon VA, Keighley MR, Dykes PW, Heppinstall K, Jaderberg M. Comparison of minimal and conventional surgery in patients with bleeding peptic ulcer: a multicentre trial. Br J Surg. 1991 Nov. 78(11):1344-5. [Medline].
Lau JY, Sung JJ, Lam YH, Chan AC, Ng EK, Lee DW, et al. Endoscopic retreatment compared with surgery in patients with recurrent bleeding after initial endoscopic control of bleeding ulcers. N Engl J Med. 1999 Mar 11. 340(10):751-6. [Medline].
Leontiadis GI, Howden CW. The role of proton pump inhibitors in the management of upper gastrointestinal bleeding. Gastroenterol Clin North Am. 2009 Jun. 38(2):199-213. [Medline].
Targownik LE, Bolton JM, Metge CJ, Leung S, Sareen J. Selective serotonin reuptake inhibitors are associated with a modest increase in the risk of upper gastrointestinal bleeding. Am J Gastroenterol. 2009 Jun. 104(6):1475-82. [Medline].
So JB, Yam A, Cheah WK, Kum CK, Goh PM. Risk factors related to operative mortality and morbidity in patients undergoing emergency gastrectomy. Br J Surg. 2000 Dec. 87(12):1702-7. [Medline].
Sadic J, Borgström A, Manjer J, Toth E, Lindell G. Bleeding peptic ulcer - time trends in incidence, treatment and mortality in Sweden. Aliment Pharmacol Ther. 2009 Aug 15. 30(4):392-8. [Medline].
Jo Y, Matsumoto T, Aoyagi K, Yano Y, Kawasaki A, Fujishima M. Endoscopic band ligation device for bleeding gastric angiodysplasia. Gastrointest Endosc. 1999 Oct. 50(4):599. [Medline].
Socrate AM, Rosati L, Locati P. Surgical treatment of aorto-enteric fistulas. Minerva Cardioangiol. 2001 Feb. 49(1):37-45. [Medline].
Young RM, Cherry KJ Jr, Davis PM, Gloviczki P, Bower TC, Panneton JM, et al. The results of in situ prosthetic replacement for infected aortic grafts. Am J Surg. 1999 Aug. 178(2):136-40. [Medline].
Deshpande A, Lovelock M, Mossop P, Denton M, Vidovich J, Gurry J. Endovascular repair of an aortoenteric fistula in a high-risk patient. J Endovasc Surg. 1999 Nov. 6(4):379-84. [Medline].
Lonn L, Dias N, Veith Schroeder T, Resch T. Is EVAR the treatment of choice for aortoenteric fistula?. J Cardiovasc Surg (Torino). 2010 Jun. 51(3):319-27. [Medline].
Burks JA Jr, Faries PL, Gravereaux EC, Hollier LH, Marin ML. Endovascular repair of bleeding aortoenteric fistulas: a 5-year experience. J Vasc Surg. 2001 Dec. 34(6):1055-9. [Medline].
Abou-Zamzam AM Jr, Bianchi C, Mazraany W, Teruya TH, Hopewell J, Vannix RS, et al. Aortoenteric fistula development following endovascular abdominal aortic aneurysm repair: a case report. Ann Vasc Surg. 2003 Mar. 17(2):119-22. [Medline].
Tseng PH, Liou JM, Lee YC, Lin LY, Yan-Zhen Liu A, Chang DC, et al. Emergency endoscopy for upper gastrointestinal bleeding in patients with coronary artery disease. Am J Emerg Med. 2009 Sep. 27(7):802-9. [Medline].
Penston JG, Wormsley KG. Review article: maintenance treatment with H2-receptor antagonists for peptic ulcer disease. Aliment Pharmacol Ther. 1992 Feb. 6(1):3-29. [Medline].
Lai KC, Lam SK, Chu KM, Wong BC, Hui WM, Hu WH, et al. Lansoprazole for the prevention of recurrences of ulcer complications from long-term low-dose aspirin use. N Engl J Med. 2002 Jun 27. 346(26):2033-8. [Medline].
Raskin JB, White RH, Jackson JE, Weaver AL, Tindall EA, Lies RB, et al. Misoprostol dosage in the prevention of nonsteroidal anti-inflammatory drug-induced gastric and duodenal ulcers: a comparison of three regimens. Ann Intern Med. 1995 Sep 1. 123(5):344-50. [Medline].
Podolsky I, Storms PR, Richardson CT, Peterson WL, Fordtran JS. Gastric adenocarcinoma masquerading endoscopically as benign gastric ulcer. A five-year experience. Dig Dis Sci. 1988 Sep. 33(9):1057-63. [Medline].
Levine JE, Leontiadis GI, Sharma VK, Howden CW. Meta-analysis: the efficacy of intravenous H2-receptor antagonists in bleeding peptic ulcer. Aliment Pharmacol Ther. 2002 Jun. 16(6):1137-42. [Medline].
Bai Y, Guo JF, Li ZS. Meta-analysis: erythromycin before endoscopy for acute upper gastrointestinal bleeding. Aliment Pharmacol Ther. 2011 Jul. 34(2):166-71. [Medline].
Barkun AN, Bardou M, Martel M, Gralnek IM, Sung JJ. Prokinetics in acute upper GI bleeding: a meta-analysis. Gastrointest Endosc. 2010 Dec. 72(6):1138-45. [Medline].
Brooks M. Poorer peptic ulcer outcomes without H. pylori etiology. Reuters Health Information. July 9, 2013. [Full Text].
Brooks M. SSRIs Linked to Upper GI Bleeds. Medscape Medical News. Available at http://www.medscape.com/viewarticle/811547. Accessed: September 30, 2012.
Chason RD, Reisch JS, Rockey DC. More favorable outcomes with peptic ulcer bleeding due to Helicobacter pylori. Am J Med. 2013 Jul 3. [Medline].
Wang YP, Chen YT, Tsai CF, et al. Short-term use of serotonin reuptake inhibitors and risk of upper gastrointestinal bleeding. Am J Psychiatry. 2014 Jan. 171 (1):54-61. [Medline].
Fujishiro M, Iguchi M, Kakushima N, et al. Guidelines for endoscopic managements of non-variceal upper gastrointestinal bleeding. Dig Endosc. 2016 Feb 22. [Medline].
- Table 1. Probable Source of GI Bleeding Within the Gut
- Table 2. Estimated Fluid and Blood Losses in Shock
- Table 3. Effect of Number of Packed Erythrocyte Transfusions on Need for Surgery and Mortality from UGIB
- Table 4. Effect of the Color of the Nasogastric Aspirate and of the Stool on UGIB Mortality Rate
- Table 5. Ulcer Characteristics and Correlations
- Table 6. Recurrent Ulcer and Postgastrectomy Syndromes After Operations for Duodenal Ulcer
- Table 7. Effects of Operations for PUD on Gastric Emptying and Motility
|Clinical Indicator||Probability of Upper GI Source||Probability of Lower GI Source|
|Blood-streaked stool||Rare||Almost certain|
|Occult blood in stool||Possible||Possible|
|Class 1||Class 2||Class 3||Class 4|
|Blood Loss, mL||Up to 750||750-1500||1500-2000||>2000|
|Blood Loss,% blood volume||Up to 15%||15-30%||30-40%||>40%|
|Pulse Rate, bpm||< 100||>100||>120||>140|
|Respiratory Rate||Normal or Increased||Decreased||Decreased||Decreased|
|Urine Output, mL/h||>35||30-40||20-30||14-20|
|Fluid Replacement, 3-for-1 rule||Crystalloid||Crystalloid||Crystalloid and blood||Crystalloid and blood|
|Number of Units Transfused||Need for Surgery, %||Mortality Rate, %|
|Nasogastric Aspirate Color||Stool Color||Mortality Rate, %|
|Clear||Brown or red||6|
|Coffee-ground||Brown or black||8.2|
|Ulcer Characteristics||Prevalence Rate, %||Rebleeding Rate, %||Surgery Rate, %||Mortality Rate, %|
|Original Operation||Recurrence Rate, %||Postgastrectomy Syndrome Rate, %||Mortality Rate, %|
|Proximal gastric vagotomy||10||5||0.1|
|Truncal vagotomy and drainage||7||20-30||< 1|
|Truncal vagotomy and antrectomy
Billroth I or Billroth II
|Truncal vagotomy and antrectomy
|Operation||Antral Innervation||Liquid Emptying||Solid Emptying|
|Proximal gastric vagotomy||Preserved||Fast||Normal|
|Truncal vagotomy and drainage||Divided||Fast||Fast|
|Truncal vagotomy and antrectomy||Divided||Fast||Fast|